Improvement of Nonsuicidal Self-Injury Following Treatment with Antipsychotics Possessing Strong D1 Antagonistic Activity: Evidence from a Report of Three Cases

Below:  Persistent remission of nonsuicidal self-injury was associated with the administration of neuroleptics possessing strong D1 receptor antagonistic activity. Shown are the courses of pharmacotherapy in three adult female patients (a–c) suffering from NSSI associated with major depression. The x-axis indicates the day of treatment. Above the x-axis, the frequency of NSSI (times per day, black bars) is shown. The y-axis indicates the doses of the different drugs administered (in mg/day). Graphs were created using the IGOR Pro 6® software (WaveMetrics, Portland, OR, USA). Flupentixol is highlighted in red. Chlorprothixene is highlighted in blue. Zuclopenthixol is highlighted in green. AMI, amitriptyline; CPT, chlorprothixene; d, day; FPX, flupentixol; GPN, gabapentin; LTG, lamotrigine; LZP, lorazepam; OZP, olanzapine; QTP, quetiapine; TPM, topiramate; TRI, trimipramine; VLX, venlafaxine; ZPT, zuclopenthixol.

There is no drug treatment for nonsuicidal self-injury (NSSI), a highly prevalent and burdensome symptom of several psychiatric diseases like posttraumatic stress disorder (PTSD), personality disorders, and major depression (MD).

Here, we present a retrospective series of three patients demonstrating a persistent remission in MD-associated NSSI in response to treatment with antipsychotics possessing marked D1 receptor antagonistic activity.

Together with previously published data from rodent models, the findings suggest a role for D1 antagonists in NSSI drug therapy and hence for the D1 receptor in NSSI pathogenesis. This conclusion is limited by the facts that the patients presented here received polypharmacy and that the D1 receptor antagonistic antipsychotics suggested here as effective ‘anti-auto-aggressants’ do not address D1 receptors only but multiple neurotransmitter receptors/systems.

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